| Project/Area Number |
17370065
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Molecular biology
|
|---|
| Research Institution | National Institute of Genetics (2006-2007)
National Institute for Basic Biology (2005) |
|---|
Principal Investigator |
KOBAYASHI Takehiko National Institute of Genetics, Department of Cell Genetics, Professor (40270475)
|
|---|
| Project Period (FY) |
2005 – 2007
|
| Project Status |
Completed (Fiscal Year 2007)
|
| Budget Amount *help |
¥15,480,000 (Direct Cost: ¥14,400,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2007: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2006: ¥4,200,000 (Direct Cost: ¥4,200,000)
Fiscal Year 2005: ¥6,600,000 (Direct Cost: ¥6,600,000)
|
|---|
| Keywords | Genome instability / Ribosomal RNA gene repeats(rDNA) / Gene amplification / Non coding RNA / DNA recombination / Cohesin / Phylogenetic footprinting / Cellular senescence / noncodingプロモーター / DNA損傷薬剤 / サイレンシング / 組み換え / 姉妹染色分体結合 / DNA修復 / 遺伝学 / ゲノム / noncoding RNA / 組換え / 姉妹染色分体 |
|---|
| Research Abstract |
The ribosomal RNA gene repeats (rDNA) is one of the most characteristic regions in eukaryotic chromosomes. The repeats consist of more than 100 tandem units occupying large part of the chromosome in most of organisms. Repeated genes families such as the ribosomal RNA genes (rDNA) are thought to be fragile sites for deletional recombination. However, as for the rDNA, cells have gene amplification system and recover copy number to the wild type level. We found a cis-essential sequence (EXP) for the amplification. In this research, I analyzed molecular mechanism of the EXP.
First, we did the phylogenetic footprinting assay in the EXP using several kinds of yeasts and found a conserved region. Interestingly, the region was a bi-directional noncoding transcriptional promoter that is reported〜20 years ago. We tested the character of the promoter and found the transcription was essential for the amplification. Interestingly, when the rDNA copy number reduces, the transcription is activated and it removes cohesin from the region. As the result, unequal sister-chromatid recombination increases and amplification is induced. Then, when the copy number reaches around the wild type level, Sir2 protein represses the transcription and by the function of recovered cohesin the unequal sister-chromatid recombination is restricted. Like these, we found the copy number regulation system, that is, Sir2 regulates rDNA copy number through E-pro transcription by changing cohesin association.
|
